Choosing the right Doct=
or

For all of this, it is paramount that we have a personal physician and s=
pecialized doctors that we trust and that we can talk openly with and =
discuss our issues and questions. To have a meaningful conversation with ou=
r doctors we need to educate ourselves on the things that we talk about, an=
d we need a doctor that treat us as a partner in our quest for=
optimum health. Doctors that treat us top down as ignorant patients won't =
help us at all.

Measuring our Well-Bein=
g

To get a holistic view of the state of our health we monitor several bio=
chemical markers and risk factors, most of them by blood, stool, urine, hai=
r, and saliva testing.

These markers serve as indicators if there is something wrong with how w=
e treat our body, the external influences that we are exposed to or our gen=
etic programming. Usually, we do not counter imbalances directly with medic=
ation like conventional medicine would suggest (e.g. treating high choleste=
rol with cholesterol-lowering drugs, which by the way is totally useless). =
It is necessary to remove the root cause for an elevated risk factor or out=
of range biochemical marker.

Tracking risk factors and biochemical markers over time gives us an exce=
llent indication how our measures like nutrition, detox, workout, mental we=
ll-being and supplementation change our body biochemistry for the better, a=
nd can be a highly motivating progress indicator in our quest for the drama=
tic extension of our healthy lifespan.

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Gut Biome

A stool sample makes it possible to analyze the distribution of the diff=
erent kinds of bacteria in our gut. Additionally, the test shows the state =
of the gut's immune system and the condition of its lining by measuring IgA=
.

Imbalances can be treated with supplementation and change in diet.=
They usually resolve once we switch to healthy nutrition, detox our body a=
nd consume enough fiber in our food. Adding pre- and probiotics to our supp=
lement regimen assists in regaining a balanced gut biome.

Chronic Inflammation

Chronic inflammation is an abnormal, long-term activation of our immune =
system. During a chronic inflammatory response, our immune system unsuccess=
fully tries to deal with an infection, injury or other disease processes. D=
amage to the tissues in our body frequently occurs during this type of infl=
ammation. Chronic, low-level inflammation is associated with common disease=
s including cancer, type II diabetes, osteoporosis, cardiovascular diseases=
, and others. It can be triggered by uric acid crystals, oxidized lipoprote=
ins, homocysteine, mitochondrial dysfunction, food toxins, gluten, and adva=
nced glycation end products (AGEs).

There are several biomarkers that we can use to detect our =
level of chronic inflammation. The two most common ones are c-reactive prot=
ein (CRP) and fibrinogen. For CRP we use the high sensitivity test (hsCRP) =
that measures CRP in the range of 0 - 10 mg/L.

Optimum hsCRP in men: < 0.55 mg/L

Optimum hsCRP in women: < 1.0 mg/L

Optimum Fibrinogen: 200 - 300 mg/dL

Implementing the building blocks of the foundation is the key to reducin=
g chronic inflammation. Additionally, supplementation can help in that regard.

Cortisol

When stressed, the body responds by increasing cortisol output from the =
adrenal glands. At normal levels cortisol is beneficial and protective by c=
ontrolling blood pressure, blood sugar levels, inflammation, as well as str=
engthening the cardiac muscle. A normal cortisol rhythm should peak in the =
morning hours and then steadily decline through the day with the lowest lev=
els at night.

An acute rise in cortisol is not necessarily unhealthy, as it is the nat=
ural adrenal response to stress. However, when stress becomes unresolved or=
chronic, cortisol is continuously elevated, and our body enters a state kn=
own as adrenal resistance.

Chronically elevated cortisol levels are both inflammatory and catabolic=
.

Cortisol levels are also related to mental acuity and can contribute to =
degenerative diseases such as dementia and Alzheimer=E2=80=99s.

DHEA, a precursor to many other hormones also relates to adrenal functio=
n as well and unfortunately can have an inverse relationship to cortisol. T=
hus, if we have chronically elevated cortisol levels, we may have proportio=
nately low DHEA, resulting in further metabolic disturbances including weig=
ht gain, poor immune function, and hormonal imbalances.

A saliva cortisol test that samples our cortisol level multiple times th=
roughout the day is the most convenient and accurate way to observe the amo=
unt of free cortisol and its daily cycle.

Like other risk factors, cortisol will usually normalize when implementi=
ng the foundation of nutrition, detox, exercise, mental well-being, and str=
ess relief. Adrenal balancing supplements like Rhodiola, Ashwagandha, =
Ginseng, and Holy basil can help us in that respect as well.

However, to make informed decisions we have to be aware of certain wides=
pread misconceptions and some lesser known facts.

Monitoring the trend is important

Conventional medicine uses arbitrary thresholds to classi=
fy people into healthy, pre-diabetic and diabetic. This is not really helpf=
ul. If a fasting blood glucose of 140 makes us diabetic, a level of 139 wil=
l not make us any healthier. In addition to the actual levels, we look out =
whether any of our values creeps upwards over time.

HbA1c is not a reliable marker for diabetes

HbA1c is supposed to measure the average level of blood glucose over a t=
hree months period by assessing how much of the blood cell's protein hemogl=
obin has bound to sugar molecules and formed AGEs. Since its value is in di=
rect relation to the average lifetime of our blood cells, HbA1c can vary va=
stly from one person to another. On average the lifetime is 90 days, but th=
e blood cells of diabetics turnover in as few as 80 days, while they live a=
s long as 140 days in non-diabetics. At the same average level of blood sug=
ar a shorter average lifetime of blood cells directly translates to a lower=
HbA1c, since the cells have less time to accumulate glycated hemoglobin pr=
oteins.

Fasting glucose goes up low-carb

Restricting carbohydrates results in a natural drop in insulin levels, w=
hich in turn activates the hormone Lipase. Fat tissue is then broken down a=
nd released into the bloodstream. These fats are taken up by our muscles, w=
hich use them as fuel. And since our muscle=E2=80=99s needs for fuel has be=
en met, it decreases its sensitivity to insulin.

On a low-carb diet a borderline high FBG of 90-105 may not cause concern=
. However, uninformed physicians might diagnose this as pre-diabetic.

Oral Glucose Tolerance Tests (OGTT) can be misleading=
p>

OGTTs are supposed to measure the performance of our glucose / insulin m=
etabolism. These are done by measuring baseline glucose and then consuming =
75 g of glucose dissolved in water. Blood glucose is then measured every 30=
minutes for up to three hours.

Unfortunately, this is a completely artificial test, stressing the body =
in a way no regular meal would. This is especially true if we are on a low-=
carb diet, where an OGTT, without consuming high amounts of carbohydrates f=
or at least three days prior to the test, would almost always indicate that=
we are diabetic, even when in perfect health.

Post Meal Glucose Levels are most relevant

Our preferred method of evaluating our glucose metabolism, apart from mo=
nitoring absolute values and trends in our regular blood draws, is tracking=
its operation while our body processes food that we regularly consume. Thi=
s can be easily done at home using either an inexpensive blood glucose mete=
r or a continuous blood glucose monitor.

When using a gl=
ucose meter we sample our glucose level before lunch and then ever=
y hour for three hours. A continuous glucose monitor will sample =
glucose levels every five minutes all day long. This is particularly conven=
ient if we want to track our response to certain kinds of food.

This will also help us to identify the most damaging situation in our gl=
ucose metabolism: blood glucose spikes after the consumption of high carb&n=
bsp; / high GL foods.

As a rule of thumb, post-meal&=
nbsp;blood glucose levels should not spike above 140 mg/dl one hour after t=
he meal, should drop below 120 mg/dl after =
two hours and return to pre-meal levels after not more than three hours.

Thyroid

The primary function of our thyroid gland and its two hormones T3 and T4=
is to regulate our metabolism by controlling the rate at which our body co=
nverts oxygen and calories to energy. In fact, the metabolic rate of every =
cell in our body is regulated by thyroid hormones, primarily T3.

The=
re is a good chance that our thyroid is either over- or under-active, due t=
o genetic variations, auto-immune reactions or our aging process. These imb=
alances directly impact our metabolism with numerous secondary effects detr=
imental to our health and well-being.

Vitamin D is produced by the body during sun exposure. However, most of =
us don't get enough of sun exposure, especially during winter.

Vitamin D can be supplemented easily and is quite inexpensive. Required =
doses range from 2.000 to 10.000 IU/day. The amount of D3 in conventional m=
ultivitamins is usually not sufficient to maintain healthy levels of 50 - 6=
0 ng/ml.

Blood Lipids

Imbalanced blood lipids, particularly cholesterol, are major risk factor=
s for our cardiovascular system. However, there are huge misconceptions on =
blood lipids, especially in the older medical community, that we have to be=
aware of to make informed decisions on our health.

LDL & HDL are not Cholesterol

Both are just transport proteins that the body uses to distribute choles=
terol where needed.

Dietary cholesterol is irrelevant

Dietary cholesterol accounts for less than 10-20% of total cholesterol i=
n our body, which manufactures almost all of its cholesterol by itself. The=
scientific myth of dietary cholesterol influencing the blood levels of cho=
lesterol originates of experimenting with animals that had an entirely diff=
erent lipid metabolism than humans. Nevertheless, these results were applie=
d 1:1 to the human realm.

There is no need at all to cut back on eggs. Quite the contrary: Eggs ar=
e among the most healthy food that we can consume.

No healthy level of "Total Cholesterol" has so far been establis=
hed

Almost unbelievable, but true nevertheless: There is no scientific proof=
for the often quoted healthy level of total cholesterol of < 200. There=
is even one Canadian study that places the healthy level of total choleste=
rol between 250 and 300.

Studies on cholesterol usually aim at the correlation of the amount of t=
otal cholesterol and the occurrence of heart disease. Unfortunately, correl=
ation is not causation. We also need to keep in mind that these relationshi=
ps are analyzed for an average population that lives on an entirely unhealt=
hy diet of sugar, wheat, and dairy.

Using total cholesterol to make a statement about one's health is about =
as accurate as to determine the health of a car by combing tire pressure, o=
il pressure, oil temperature, water temperature and water pressure in a sin=
gle number and flashing it one on the dashboard.

Conventional LDL & VLDL measurement is no measurement at all=

The LDL values reported by our blood test are almost always only calcula=
ted and never actually measured at all. To avoid the much more costly corre=
ct LDL measurement values are estimated by one of two formulas:

VLDL is often not measured but only calculated by dividing triglycerides=
by 5

Reporting a single number for LDL completely misses the point

LDL comes in three different particle sizes and unfortunately, in tradit=
ional reporting, no distinction between the various LDL particle sizes is m=
ade at all. However, only the smallest size, type B LDL, is the real risk f=
actor for heart disease. LDL-B oxidizes quickly and is small enough to get =
stuck in between cells. Oxidized LDL-B in conjunction with a chronic system=
ic inflammation (measured by CRP) triggers an immune reaction causing the p=
articles to be eaten by our immune systems macrophages which in turn get bl=
oated. The bloated macrophages start to accumulate in the walls of our bloo=
d vessels - up to a point where the vessel wall ruptures, releasing a blob =
of bloated macrophages into the bloodstream, blocking the blood vessel and =
causing a heart attack or stroke.

Two people with the same calculated LDL can have an entirely different r=
isk profile for heart disease. One might be perfectly healthy, the other on=
e in grave danger.

Calculated LDL can go up on a healthy diet

When we switch from an unhealthy, toxic, carb-loaded diet based on wheat=
, sugar, and dairy to a healthy, evolutionary diet and implement the other =
building blocks of the foundation as well, the distribution of our LDL=
particle size will shift from high-risk factor small particle LDLs to the =
good large LDLs.

Unfortunately, standard LDL measurement under-represents small LDLs and =
will mostly show the increased number of large LDLs. This leads to an incre=
ased "measured" total LDL despite the decrease in high-risk factor small LD=
L.

Unaware physicians will diagnose this as a sign of an increased risk fac=
tor even so quite the opposite is true. They might even suggest counteracti=
ng with medication to lower LDL.

No use for drugs to lower LDL

Imbalanced cholesterol levels are not a root cause for heart disease, bu=
t secondary effects and an indicator for imbalances in the metabolism. They=
are the consequence of an unhealthy lifestyle, with excess carbohydrates, =
lack of exercise, bad detox, negative stress and to some extent of our gene=
tics.

Combining this insight with the knowledge how LDL is "measured" it becom=
es apparent that using drugs to lower cholesterol makes little sense and co=
uld be compared to putting at sticker over a red light on the das=
hboard.

Correlation studies have identified two other lipoprotein sub classes th=
at are associated with an increased risk of cardiovascular disease.

Optimum lipoprotein A - Lp(a): < 20 mg / dL

Optimum lipoprotein A2 - Lp(a2): < 235 mg / dL

The foundation is the key

Once we implement the building blocks of the foundation, we see our rele=
vant lipid blood markers normalize to healthy levels. And even if some of t=
hem are a bit off compared to the (unhealthy) population average (most prob=
ably due to our genetic makeup), we must remember that they are only a subs=
et of the risk factors attributed to lead to heart disease. We still have a=
lot of control over the other factors as well.

Glycation

Advanced glycation end products (AGEs) are molecules that form when suga=
r molecules bind to proteins and lipids in the body. This process is called=
glycation. Glycation, unfortunately, is a normal part of agi=
ng, it is far from desirable.

AGEs are one of the major causes why our body ages

AGEs cross-link with themselves and the surrounding tissue, forming unbr=
eakable bonds and stiffening our tissue as we age. Rigid blood vessels due =
to AGEs lead to age-related high blood pressure since the vessels cannot ex=
pand anymore when the heart pumps blood. Stiffening of our heart muscl=
e results in a loss of power, volume and thus the ability to pump blood, ox=
ygen, and nutrition through our body. Stiffening of our lung and the connec=
ted muscles leads to loss of lung capacity. Cross-linking of the collagen i=
n our skin leads to wrinkles and age spots. Cross-linking in the lense=
s of our eyes causes clouding and thus a loss of vision. AGEs contribute to=
cataracts, atherosclerosis, kidney failure and are a contributing factor i=
n the development of various age-related diseases.

Tracking Glycation

We can track the level of glycation to some extent by monitoring hemoglo=
bin A1c (HbA1c), that measures the percentage of glycated hemoglobin protei=
ns in our blood cells. An elevated or an upward trending =
HbA1c over time is a serious risk factor.

Healthy HbA1c: < 5.3 %

Optimum HbA1c: < 5 %

We have to keep in mind that HbA1c can vary from person to person. I=
ts measurement is about the average lifetime of our blood cells. On average=
that is 90 days but may vary considerably from person to person. With the =
same rate of glycation, a shorter average lifetime of blood cells directly =
translates to a lower HbA1c, since the cells have less time to accumulate A=
GEs.

Limiting Glycation

We want to keep the rate of glycation in our body as low as possible. We=
do this by preventing or blood sugar from spiking, implementing a proper d=
iet and exercise regularly. Additionally, we can supplement with Benfotiami=
ne (a form of vitamin B1), pyridoxal 5'-phosphate (a form of vitamin B6) an=
d Carnosine, which all reduce glycation reactions that occur in our body.=
p>

We have to be aware that not only we make our own AGEs, we also consume =
pre-manufactured AGEs with our food. AGE form from sugar and fat under exce=
ss heat, e.g., in baking or on a BBQ, especially if the food is partly burn=
ed.

A Word on Fructose

Fructose (60% of the carbohydrates in fruit), is seven times more reacti=
ve than glucose (the primary carbohydrate in rice or sweet potatoes) =
in regard to forming AGEs.

As opposed to glucose, which can be used by all the cells of our body, f=
ructose can only be processed by our liver. Hence, excess fruc=
tose, which cannot immediately be handled by our liver, floats in our blood=
stream, readily forming AGEs until the liver can take care of it.

Additionally, our liver has only a limited capacity to store sugars. Exc=
ess fructose that cannot be stored in our liver is converted and directly t=
ransferred to our fat cells for storage.

Thus, we want to keep excess fructose, which our liver cannot process an=
d store to an absolute minimum. If we consume fruits, which are our primary=
source of fructose, we do so in the morning, when our liver's storage capa=
city for sugars is still depleted from the night. We always consume the who=
le fruit, as opposed to fruit juice, since the fiber in them slows digestio=
n and absorption of fructose into the bloodstream. We avoid fruit juices, e=
ven freshly squeezed ones since they lack that fiber.

In the Future

Unfortunately, our body can not break-up or get rid of formed AGEs. Righ=
t now all we can do is try to limit their formation and accumulation.

Scientists are already developing technologies that will allow us to bre=
ak-up cross-linked AGEs and return stiffened tissue to its youthful state. =
This would result in real rejuvenation techniques, undoing one of the leadi=
ng causes of aging.

Acid Balance

Our body has to keep a very tight regulation of its alkaline-acidic bala=
nce. The pH of our blood has to remain within a tiny window of 7.35 - 7.45.=
Even slight deviations have significant health implications.

Base excess (BE) indicates the amount of bicarbonat=
e in our system used to balance pH. A negative BE is reflecting a base defi=
cit in our blood and is equivalent to an acid excess. A value outside the n=
ormal range (-2 to +2 mEq) suggests a metabolic disorder.

The most common reason for an imbalance is excess a=
cid due to bad diet, alcohol, coffee, environmental toxins, smoking, stress=
or lack of sleep.

Fatty Acids

We analyze the distribution and possible imbalances of fatty acids in ou=
r body on the cellular level =E2=80=94 especially Omega 3, 6, 9 and saturat=
ed fats. It's really motivating to see these values change for the better o=
nce we implement a healthy diet, the other building blocks of the foundatio=
n and a basic supplementation program.

Micronutrient=
s on the Cellular Level

Due to genetic mutations that are present in every one of us, we all pro=
cess food and nutrients with different efficiency, sometimes to an order of=
a magnitude. A balanced diet and supplements do not necessarily assure tha=
t our cells benefit at the optimum levels. Blood levels alone don't provide=
the real picture either since our deficit might be related to inadequate t=
ransport or reduced cellular uptake of a particular compound.

Fortunately, there is a test that allows us to measure the levels of the=
essential micro nutrients within in the cells, which makes it=
possible to detect deficiencies directly at a cellular level - and counter=
them by supplementing the missing compound.